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Neurology International Jun 2023(1) Background: Parkinson's disease (PD) is a relatively common and complex pathology, and some of its mechanisms remain to be elucidated. Change in host microbiota is... (Review)
Review
(1) Background: Parkinson's disease (PD) is a relatively common and complex pathology, and some of its mechanisms remain to be elucidated. Change in host microbiota is related to the pathophysiology of numerous diseases. This systematic review aims to gather existing data on the occidental hemisphere, compare it, and search for any significant association between Parkinson's disease and gut microbiota dysbiosis. (2) Methods: Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) and Meta-analyses Of Observational Studies in Epidemiology (MOOSE) protocols were used for this systematic review. PubMed was used as the database search engine. Of the 166 studies found, only 10 were used, as they met our inclusion criteria: case-control studies, studies that assessed the correlation of PD and gut microbiome, studies that took place in occidental regions, and studies that were performed on humans and were written in English. The Newcastle-Ottawa Scale was used as the assessment tool for overall risk of bias in this systematic review. (3) Results: The studies analyzed were divided into three geographic areas: Region 1: United States of America and Canada; Region 2: Germany, Ireland, and Finland; and Region 3: Italy; based on geographical similarities among these populations. The following statistically significant results were described in PD patients, compared with non-PD controls. In the first region, a significant increase in the following bacteria was seen: 1. Phylum: Actinobacteriota and its Genus: ; 2. Phylum: Verrucomicrobiota and its Genus: ; 3. Genus: , , , and of the Phylum: Firmicutes; 4. Family: of Phylum: Firmicutes; 5. Phylum: Bacteroidetes and its Genus: ; 6. Phylum: Proteobacteria. A significant decrease was described in the Family: and its Genus: , , and , which belong to the Phylum: Firmicutes. In the second region, a raised number of: 1. Phylum: Verrucomicrobiota, its Genus: , and its Species: ; 2. Family: of the Phylum: Verrucomicrobiota; 3. Genus: and of the Phylum: Firmicutes; 4. Family: of the Phylum: Firmicutes; 5. Family: of the Phylum: Bacteroidetes; 6. Genus: of the Phylum: Actinobacteriota; 7. Species: of the Phylum: Thermodesulfobacteriota, was identified. Only one Genus: of the Phylum: Bacteroidetes was decreased. In the third and last region, an augmented number of these bacteria were found: 1. Phylum: Verrucomicrobiota and its Genus: ; 2. Family: and of the Phylum: Actinobacteriota; 3. Phylum: Firmicutes and its Family: and ; 4. Family: and its Genus: , of the Phylum: Firmicutes; 5. Genus: and , of the Phylum: Firmicutes; 6. Phylum: Proteobacteria, its Family: , and the Genus: , , , and ; 7. Genus: of the Phylum: Bacteroidetes. In contrast, a significant decrease in 1. Phylum: Firmicutes, its Family: , and its Genus: and 2. Genus: of the Phylum: Firmicutes, was described. (4) Conclusion: A significant gut dysbiosis, involving multiple bacterial taxa, was found in PD patients compared to healthy people in the occidental regions. However, more studies are needed to find the precise pathophysiologic involvement of other groups of pathogens, such as fungi and parasites, in the development and progression of PD.
PubMed: 37368331
DOI: 10.3390/neurolint15020047 -
Neurology and Therapy Oct 2023The causal association between the gut microbiome and the risk of intracranial aneurysm (IA), subarachnoid hemorrhage (SAH), and unruptured aneurysm (uIA) is unclear.
INTRODUCTION
The causal association between the gut microbiome and the risk of intracranial aneurysm (IA), subarachnoid hemorrhage (SAH), and unruptured aneurysm (uIA) is unclear.
METHODS
The single nucleotide polymorphisms concerning gut microbiome were retrieved from the gene-wide association study (GWAS) of the MiBioGen consortium. The summary-level datasets of IA and SAH were obtained from the GWAS meta-analysis of the International Stroke Genetics Consortium (ISGC). Inverse variance weighting (IVW) was utilized as the primary method, complemented with sensitivity analyses for pleiotropy and increasing robustness.
RESULTS
Five, seven, and six bacterial traits were found to have a causal effect on IA, SAH, and uIA, respectively (IVW, all P < 0.05). Family.Porphyromonadaceae and genus.Bilophila were common protective bacterial features for both SAH and uIA. The heterogeneity and pleiotropy analyses confirmed the robustness of IVW results.
CONCLUSION
Our study demonstrates that gut microbiomes may exert therapeutic effects on IA, uIA, and SAH, providing clinical implications for the development of novel biomarkers and therapeutic targets.
PubMed: 37440166
DOI: 10.1007/s40120-023-00525-1 -
Journal of Gastrointestinal Oncology Aug 2018Colorectal cancer (CRC) is the third most common newly diagnosed cancer in both men and women in the Unites States. Colonoscopy has become increasingly popular in CRC... (Review)
Review
Colorectal cancer (CRC) is the third most common newly diagnosed cancer in both men and women in the Unites States. Colonoscopy has become increasingly popular in CRC screening and represents the gold standard for detecting and removing pre-cancerous lesions. Although colonoscopy is considered a relatively safe procedure, it is invasive and bowel preparation can be challenging for patients. As interest in the gut microbiome has expanded, there have been new links established between bacteria and the development of CRC. These developing associations could prove to be a useful adjunct to colonoscopy for CRC screening in the future. This review examines current research evaluating multiple proposed pathogenic microorganisms including sulfidogenic bacteria such as , as well as , and . This discussion primarily focuses on bacterial pathogenesis, evidence of association with CRC, and the proposed mechanisms of carcinogenesis.
PubMed: 30151274
DOI: 10.21037/jgo.2018.04.07 -
Frontiers in Oncology 2022Immune checkpoint inhibitors (ICIs) targeting programmed cell death protein 1 (PD-1) have been widely used in treating different malignancies. Several studies have...
BACKGROUND
Immune checkpoint inhibitors (ICIs) targeting programmed cell death protein 1 (PD-1) have been widely used in treating different malignancies. Several studies have reported that the gut microbiota modulates the response and adverse events (AEs) to ICIs in melanoma, non-small cell lung cancer (NSCLC), renal cell cancer and hepatocellular carcinoma, but data on other cancer types and ICI combination therapy are limited.
METHODS
Stool samples were collected from patients with cancer who received anti-PD-1 and chemotherapy combination treatment and were analyzed by fecal metagenomic sequencing. The microbiota diversity and composition were compared between the responder (R) and non-responder (NR) groups and the AE vs. the non-AE (NAE) groups. In addition, associated functional genes and metabolic pathways were identified.
RESULTS
At baseline, the microbiota diversity of the groups was similar, but the genera , , and were enriched in the R group, whereas and 11 species of were enriched in the NR group. At 6 weeks, the beta diversity was significantly different between the R and NR groups. Further analysis found that 35 genera, such as , , , , , , and and several genera of the family, were frequently distributed in the R group, whereas 17 genera, including , , , and and several genera of the and families, were more abundant in the NR group. A total of 66 and 52 Kyoto Encyclopedia of Genes and Genomes (KEGG) orthologs (KOs) were significantly enriched in the R and NR groups, respectively. In addition, pathway analysis revealed functional differences in the gut microbacteria in the R group, including the enrichment of anabolic pathways and DNA damage repair (DDR) pathways. Dynamic comparisons of the bacterial composition at baseline, 6 weeks, and 12 weeks showed that the abundance of significantly increased in the R group at 6 weeks and the abundance of and significantly increased in the NR group at 12 weeks. Linear discriminant analysis effect size analysis indicated that bacteria of , especially , were enriched in the NAE group, whereas flora of , such as , , and , were enriched in the AE group.
CONCLUSION
Beta diversity and differences in the gut microbiota modulated AEs and the response to anti-PD-1 blockade combined with chemotherapy, by regulating related anabolic and DDR pathways. Dynamic changes in the intestinal microbiome may predict the efficacy of PD-1 inhibitor-based therapy.
PubMed: 36387171
DOI: 10.3389/fonc.2022.887383 -
Anaerobe Dec 2022We report a rare case of polymicrobial anaerobic bacteremia caused by four different gut anaerobes: Bacteroides fragilis, Eggerthella lenta, Bilophila wadsworthia, and...
Polymicrobial anaerobic sepsis due to Bacteroides fragilis, Eggerthella lenta, Ruminoccocus gnavus, and Bilophila wadsworthia in a patient with myeloproliferative neoplasm.
We report a rare case of polymicrobial anaerobic bacteremia caused by four different gut anaerobes: Bacteroides fragilis, Eggerthella lenta, Bilophila wadsworthia, and Ruminococcus gnavus. Early initiation of appropriate therapy and species identification with matrix assisted laser desorption time-of-flight mass spectrometry (MALDI-TOF MS) resulted in full recovery from the infection. Our case highlights the clinical significance of polymicrobial cultures and the importance of performing anaerobic cultures for blood specimens to ensure proper identification and treatment.
Topics: Humans; Bacteroides fragilis; Bilophila; Anaerobiosis; Neoplasms; Bacterial Infections; Bacteria, Anaerobic; Bacteremia; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
PubMed: 36108892
DOI: 10.1016/j.anaerobe.2022.102641 -
Journal of Clinical Microbiology Feb 2000The influence of growth medium and incubation conditions on the detection of Bilophila wadsworthia beta-lactamase was tested with Cefinase and Cefinase Plus disks. The... (Comparative Study)
Comparative Study
The influence of growth medium and incubation conditions on the detection of Bilophila wadsworthia beta-lactamase was tested with Cefinase and Cefinase Plus disks. The tests involved aerobic and anaerobic incubation with conventional disk and quantitative tube assays. The production of beta-lactamase was correlated with penicillin G, ampicillin, and ampicillin-sulbactam MICs and inhibition zones on penicillin (2-U) disks. The strains were grown on (i) brucella agar (brucella), (ii) brucella agar supplemented with 1% pyruvate (brucella-pyruvate), and (iii) brucella agar supplemented with 1% taurine (brucella-taurine). With the aerobic disk assay, 100, 100, and 7% of strains were positive after 30 min from growth on brucella-pyruvate, brucella, and brucella-taurine plates, respectively; of strains grown on brucella-taurine, 54% remained negative by the Cefinase assay, and 23% remained negative by the Cefinase Plus assay at 2 h. In quantitative assays, the strains became positive after 30 min from brucella-pyruvate plates and after 1 h from brucella plates. The intensities of the reactions were strongest with brucella-pyruvate plates under anaerobic test conditions. Anaerobic incubation enhanced beta-lactamase detection of growth on brucella-taurine: at 3 h, 85% of strains were positive in comparison to 38% with aerobic incubation. All beta-lactamase-negative strains were susceptible to penicillin G and ampicillin; all beta-lactamase-positive strains were resistant to ampicillin and, with the exception of two strains, penicillin G. In conclusion, beta-lactamase production correlated with susceptibility to penicillin G and ampicillin. Brucella agar supplemented with 1% pyruvate was the most reliable medium for testing B. wadsworthia beta-lactamase, and anaerobic incubation expedited positive results. Brucella agar supplemented with taurine was unsuitable for B. wadsworthia beta-lactamase testing. Cefinase and Cefinase Plus results were in agreement, but Cefinase Plus yielded faster reactions.
Topics: Aerobiosis; Anaerobiosis; Cephalosporins; Culture Media; Gram-Negative Anaerobic Bacteria; Gram-Negative Bacterial Infections; Humans; Indicators and Reagents; Microbial Sensitivity Tests; Penicillins; beta-Lactamases
PubMed: 10655376
DOI: 10.1128/JCM.38.2.733-736.2000 -
Disease Markers 2022The study analyzed gut microflora's composition and investigated the associations between the associations between gut dysbiosis and inflammatory indicators in pediatric...
BACKGROUND
The study analyzed gut microflora's composition and investigated the associations between the associations between gut dysbiosis and inflammatory indicators in pediatric patients with acute appendicitis.
METHODS
High-throughput sequencing and bioinformatics analysis were used to investigate the composition and diversity of gut microflora in 20 pediatric patients with acute appendicitis and 11 healthy children. Endpoints measured were operational taxonomic units (OTU) of gut microflora. The OTU and its abundance analysis, sample diversity analysis, principal component analysis of samples, differential analysis, and analysis of biomarkers were performed.
RESULTS
Overall fecal microbial richness and diversity were similar in patients and controls. Yet richness within the group of Bilophila, Eggerthella, Clostridium, Parvimonas, Megasphaera, Atopobium, Phascolarctobacterium, Adlercreutzia, Barnesiella, Klebsiella, Enterococcus, and Prevotella genera was higher in patients. Adlercreutzia was significantly positively correlated with IL-10, while the three other genera, comprising Klebsiella, Adlercreutzia, and Prevotella, were positively correlated with B cells level.
CONCLUSION
Gut microbiome components are significantly different in pediatric patients with acute appendicitis and healthy children. The differential abundance of some genera is correlated with the production of inflammatory markers in appendicitis.
Topics: Appendicitis; Biomarkers; Child; Dysbiosis; Feces; Gastrointestinal Microbiome; Humans
PubMed: 35845131
DOI: 10.1155/2022/1059445 -
Canadian Journal of Veterinary Research... Jul 2003Proliferative enteropathy is an important enteric disease caused by Lawsonia intracellularis. A wide range of host species can be infected by the same bacterium, yet the...
Proliferative enteropathy is an important enteric disease caused by Lawsonia intracellularis. A wide range of host species can be infected by the same bacterium, yet the clinico-pathologic features among these hosts remains almost identical. The disease has been recognized regularly among ratites, but not in other avian families, such as galliforms, even though these suffer uncharacterized enteric conditions. Fresh ileum-colon contents were obtained from 228, 3- to 8-week-old chickens with enteric disease, kept at 14 large commercial farms in the southern USA. DNA was extracted from each sample and subjected to polymerase chain reactions (PCR) with primers specific to eubacterial DNA, L. intracellularis, and Bilophila wadsworthia. All chicken samples were positive for eubacterial DNA, 29 chickens (13%) were positive for B. wadsworthia DNA, and none were positive for L. intracellularis DNA. Given the ubiquitous nature of L. intracellularis, we consider it likely that some avian families do not carry the necessary mechanism for L. intracellularis viability. Bilophila wadsworthia appears to be a consistent member of the colonic flora of some host animals. Neither bacterium appears to be associated with malabsorption syndromes in chickens.
Topics: Animals; Chickens; DNA, Bacterial; Deltaproteobacteria; Desulfovibrionaceae Infections; Gram-Negative Bacterial Infections; Lawsonia Bacteria; Malabsorption Syndromes; Polymerase Chain Reaction; Poultry Diseases
PubMed: 12889732
DOI: No ID Found -
Investigative Ophthalmology & Visual... Jun 2023To explore the mechanisms relating the gut microbiome (GM) to age-related macular degeneration (AMD), as they remain unclear. GM taxa that appear to act within the...
PURPOSE
To explore the mechanisms relating the gut microbiome (GM) to age-related macular degeneration (AMD), as they remain unclear. GM taxa that appear to act within the gut-retina axis may affect the risk of AMD.
METHODS
Single-nucleotide polymorphisms (SNPs) of 196 GM taxa were obtained from the MiBioGen consortium, and a Mendelian randomization (MR) study was carried out to estimate the causality between GM taxa and AMD (defined as an endpoint based on ICD-9 and ICD-10). Using the data from the FinnGen consortium (6157 patients and 288,237 controls), we explored the GM taxa for causality and verified the results at the replication stage based on the MRC-IEU consortium (3553 cases and 147,089 controls). Inverse variance weighting (IVW) was the main method used to analyze causality, and the MR results were verified using heterogeneity tests and pleiotropy tests.
RESULTS
According to the MR results, order Rhodospirillales (P = 3.38 × 10-2), family Victivallaceae (P = 3.14 × 10-2), family Rikenellaceae (P = 3.58 × 10-2), genus Slackia (P = 3.15 × 10-2), genus Faecalibacterium (P = 3.01 × 10-2), genus Bilophila (P = 1.11 × 10-2), and genus Candidatus Soleaferrea (P = 2.45 × 10-2) were suggestively associated with AMD. In the replication stage, only order Rhodospirillales (P = 0.03) passed validation. The heterogeneity (P > 0.05) and pleiotropy (P > 0.05) tests in two stages confirmed the robustness of the MR results.
CONCLUSIONS
We confirmed that order Rhodospirillales influenced the risk of AMD based on the gut-retina axis, providing new impetus for the development of the GM as an intervention to prevent the occurrence and development of AMD.
Topics: Humans; Gastrointestinal Microbiome; Macular Degeneration; Retina; Causality; Actinobacteria
PubMed: 37314756
DOI: 10.1167/iovs.64.7.22 -
Shock (Augusta, Ga.) Apr 2023Background: Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in the United States, with an annual cost of 60 billion dollars. There is...
Background: Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in the United States, with an annual cost of 60 billion dollars. There is evidence suggesting that in the post-TBI period, the gastrointestinal tract plays a central role in driving organ and immune dysfunction and may be the source of increased circulating proinflammatory mediators. In this study, we examined systemic inflammation and bacterial dysbiosis in patients who sustained a TBI with or without polytrauma. Using a mouse model of TBI, we further show how neuroinflammation after TBI is potentially linked to disruptions in gut homeostasis such as intestinal transit and inflammation. Methods: During a study of trauma patients performed from September 1, 2018, to September 1, 2019, at a single, level 1 trauma center, TBI patients aged 21 to 95 years were enrolled. Patients were categorized as TBI based on evidence of acute abnormal findings on head computed tomographic scan, which was a combination of isolated TBI and TBI with polytrauma. Blood and stool samples were collected between 24 h and 3 days after admission. Twelve plasma samples and 10 fecal samples were used for this study. Healthy control samples were obtained from a healthy control biobank. We examined systemic inflammation and bacterial changes in patients who sustained a TBI. In addition, TBI was induced in 9- to 10-week-old male mice; we assessed neuroinflammation, and intestine transit (motility) and bacterial changes 24 h after TBI. Results: When compared with healthy controls, TBI patients had increased systemic inflammation as evidenced by increased levels of IFN-γ and MCP-1 and a trend toward an increase of IL-6 and IL-8 ( P = 0.0551 and P = 0.0549), respectively. The anti-inflammatory cytokine, IL-4, was also decreased in TBI patients. Although there was a trend of an increase in copy number of Enterobacteriaceae and a decrease in copy number of Lactobacillus in both patients and mice after TBI, these trends were not found to be significantly different. However, TBI significantly increased the copy number of another potential pathogenic bacteria Bilophila wadsworthia in TBI patients compared with healthy controls. After a moderate TBI, mice had increased expression of TNF-α, IL-6 and IL-1β, CXCL1, s100a9, and Ly6G and decreased IL-10 in the brain lesion after TBI. This accompanied decreased transit and increased TNF-α in the small intestine of mice after TBI. Conclusions: Our findings suggest that TBI increases systemic inflammation, intestinal dysfunction, and neuroinflammation. More studies are needed to confirm whether changes in intestinal motility play a role in post-TBI neuroinflammation and cognitive deficit.
Topics: Male; Humans; Interleukin-6; Tumor Necrosis Factor-alpha; Neuroinflammatory Diseases; Brain Injuries, Traumatic; Inflammation; Multiple Trauma
PubMed: 36645886
DOI: 10.1097/SHK.0000000000002082